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Physiological Reviews Jul 2017Dental enamel is the hardest and most mineralized tissue in extinct and extant vertebrate species and provides maximum durability that allows teeth to function as... (Review)
Review
Dental enamel is the hardest and most mineralized tissue in extinct and extant vertebrate species and provides maximum durability that allows teeth to function as weapons and/or tools as well as for food processing. Enamel development and mineralization is an intricate process tightly regulated by cells of the enamel organ called ameloblasts. These heavily polarized cells form a monolayer around the developing enamel tissue and move as a single forming front in specified directions as they lay down a proteinaceous matrix that serves as a template for crystal growth. Ameloblasts maintain intercellular connections creating a semi-permeable barrier that at one end (basal/proximal) receives nutrients and ions from blood vessels, and at the opposite end (secretory/apical/distal) forms extracellular crystals within specified pH conditions. In this unique environment, ameloblasts orchestrate crystal growth via multiple cellular activities including modulating the transport of minerals and ions, pH regulation, proteolysis, and endocytosis. In many vertebrates, the bulk of the enamel tissue volume is first formed and subsequently mineralized by these same cells as they retransform their morphology and function. Cell death by apoptosis and regression are the fates of many ameloblasts following enamel maturation, and what cells remain of the enamel organ are shed during tooth eruption, or are incorporated into the tooth's epithelial attachment to the oral gingiva. In this review, we examine key aspects of dental enamel formation, from its developmental genesis to the ever-increasing wealth of data on the mechanisms mediating ionic transport, as well as the clinical outcomes resulting from abnormal ameloblast function.
Topics: Ameloblasts; Amelogenesis; Animals; Dental Enamel; Dental Enamel Proteins; Evolution, Molecular; Genetic Predisposition to Disease; Humans; Oral Health; Phenotype; Species Specificity; Tooth Abnormalities; Tooth Diseases
PubMed: 28468833
DOI: 10.1152/physrev.00030.2016 -
Australian Dental Journal Jun 2013Developmental enamel defects, presenting as enamel hypoplasia or opacities are caused by damage or disruption to the developing enamel organ as a result of inherited and... (Review)
Review
Developmental enamel defects, presenting as enamel hypoplasia or opacities are caused by damage or disruption to the developing enamel organ as a result of inherited and acquired systemic conditions. The high prevalence of these defects in the primary dentition demonstrates the vulnerability of the teeth to changes in the pre- and postnatal environment. The presence of enamel hypoplasia increases the risk of primary teeth to early childhood caries and tooth wear as the defective enamel is thinner, more plaque retentive and less resistant to dissolution in acid compared to normal enamel. The purpose of this paper was to critically review the aetiology and clinical complications of developmental enamel defects in the primary dentition and propose recommendations for the clinical management of affected teeth.
Topics: Child, Preschool; Dental Caries; Dental Enamel; Dental Enamel Hypoplasia; Female; Humans; Tooth Attrition; Tooth Wear; Tooth, Deciduous
PubMed: 23713631
DOI: 10.1111/adj.12039 -
Journal of Pharmacy & Bioallied Sciences Apr 2015Ameloblastoma is a benign odontogenic tumor generally present in the jaw bone. The tumor originates from the residual epithelium of the tooth germ, epithelium of... (Review)
Review
Ameloblastoma is a benign odontogenic tumor generally present in the jaw bone. The tumor originates from the residual epithelium of the tooth germ, epithelium of odontogenic cysts stratified squamous epithelium and epithelium of the enamel organ. It represents approximately 1% of oral tumors. About 80% of ameloblastomas occur in the mandible mainly the third molar region and the remaining 20% in the upper jaw. Ameloblastoma clinically appears as an aggressive odontogenic tumor, often asymptomatic and slow-growing, with no evidence of swelling. This article deals with a complete review on ameloblastoma.
PubMed: 26015700
DOI: 10.4103/0975-7406.155891 -
The Journal of Physiology May 2017Dental enamel is one of the most remarkable examples of matrix-mediated biomineralization. Enamel crystals form de novo in a rich extracellular environment in a... (Review)
Review
Dental enamel is one of the most remarkable examples of matrix-mediated biomineralization. Enamel crystals form de novo in a rich extracellular environment in a stage-dependent manner producing complex microstructural patterns that are visually stunning. This process is orchestrated by specialized epithelial cells known as ameloblasts which themselves undergo striking morphological changes, switching function from a secretory role to a cell primarily engaged in ionic transport. Ameloblasts are supported by a host of cell types which combined represent the enamel organ. Fully mineralized enamel is the hardest tissue found in vertebrates owing its properties partly to the unique mixture of ionic species represented and their highly organized assembly in the crystal lattice. Among the main elements found in enamel, Ca is the most abundant ion, yet how ameloblasts modulate Ca dynamics remains poorly known. This review describes previously proposed models for passive and active Ca transport, the intracellular Ca buffering systems expressed in ameloblasts and provides an up-dated view of current models concerning Ca influx and extrusion mechanisms, where most of the recent advances have been made. We also advance a new model for Ca transport by the enamel organ.
Topics: Ameloblasts; Animals; Biological Transport; Calcium; Calcium Signaling; Dental Enamel; Humans
PubMed: 27510811
DOI: 10.1113/JP272775 -
Calcified Tissue International Nov 2017Amelogenesis (tooth enamel formation) is a biomineralization process consisting primarily of two stages (secretory stage and maturation stage) with unique features.... (Review)
Review
Amelogenesis (tooth enamel formation) is a biomineralization process consisting primarily of two stages (secretory stage and maturation stage) with unique features. During the secretory stage, the inner epithelium of the enamel organ (i.e., the ameloblast cells) synthesizes and secretes enamel matrix proteins (EMPs) into the enamel space. The protein-rich enamel matrix forms a highly organized architecture in a pH-neutral microenvironment. As amelogenesis transitions to maturation stage, EMPs are degraded and internalized by ameloblasts through endosomal-lysosomal pathways. Enamel crystallite formation is initiated early in the secretory stage, however, during maturation stage the more rapid deposition of calcium and phosphate into the enamel space results in a rapid expansion of crystallite length and mineral volume. During maturation-stage amelogenesis, the pH value of enamel varies considerably from slightly above neutral to acidic. Extracellular acid-base balance during enamel maturation is tightly controlled by ameloblast-mediated regulatory networks, which include significant synthesis and movement of bicarbonate ions from both the enamel papillary layer cells and ameloblasts. In this review we summarize the carbonic anhydrases and the carbonate transporters/exchangers involved in pH regulation in maturation-stage amelogenesis. Proteins that have been shown to be instrumental in this process include CA2, CA6, CFTR, AE2, NBCe1, SLC26A1/SAT1, SLC26A3/DRA, SLC26A4/PDS, SLC26A6/PAT1, and SLC26A7/SUT2. In addition, we discuss the association of miRNA regulation with bicarbonate transport in tooth enamel formation.
Topics: Amelogenesis; Animals; Anion Transport Proteins; Bicarbonates; Biological Transport; Carbonic Anhydrases; Chloride-Bicarbonate Antiporters; Cystic Fibrosis Transmembrane Conductance Regulator; Dental Enamel; Humans; MicroRNAs; Sodium-Bicarbonate Symporters
PubMed: 28795233
DOI: 10.1007/s00223-017-0311-2 -
Stem Cell Research & Therapy Sep 2022Dental follicles are necessary for tooth eruption, surround the enamel organ and dental papilla, and regulate both the formation and resorption of alveolar bone. Dental... (Review)
Review
Dental follicles are necessary for tooth eruption, surround the enamel organ and dental papilla, and regulate both the formation and resorption of alveolar bone. Dental follicle progenitor cells (DFPCs), which are stem cells found in dental follicles, differentiate into different kinds of cells that are necessary for tooth formation and eruption. Runt-related transcription factor 2 (Runx2) is a transcription factor that is essential for osteoblasts and osteoclasts differentiation, as well as bone remodeling. Mutation of Runx2 causing cleidocranial dysplasia negatively affects osteogenesis and the osteoclastic ability of dental follicles, resulting in tooth eruption difficulties. Among a variety of cells and molecules, Nel-like molecule type 1 (Nell-1) plays an important role in neural crest-derived tissues and is strongly expressed in dental follicles. Nell-1 was originally identified in pathologically fused and fusing sutures of patients with unilateral coronal synostosis, and it plays indispensable roles in bone remodeling, including roles in osteoblast differentiation, bone formation and regeneration, craniofacial skeleton development, and the differentiation of many kinds of stem cells. Runx2 was proven to directly target the Nell-1 gene and regulate its expression. These studies suggested that Runx2/Nell-1 axis may play an important role in the process of tooth eruption by affecting DFPCs. Studies on short and long regulatory noncoding RNAs have revealed the complexity of RNA-mediated regulation of gene expression at the posttranscriptional level. This ceRNA network participates in the regulation of Runx2 and Nell-1 gene expression in a complex way. However, non-study indicated the potential connection between Runx2 and Nell-1, and further researches are still needed.
Topics: Bone Remodeling; Calcium-Binding Proteins; Cell Differentiation; Core Binding Factor Alpha 1 Subunit; Dental Sac; Humans; Osteogenesis; RNA; Stem Cells; Tooth Eruption; Transcription Factors
PubMed: 36175952
DOI: 10.1186/s13287-022-03140-3 -
Journal of Dental Research Nov 2018Cdc42, a Rho family small GTPase, regulates cytoskeleton organization, vesicle trafficking, and other cellular processes in development and homeostasis. However, Cdc42's...
Cdc42, a Rho family small GTPase, regulates cytoskeleton organization, vesicle trafficking, and other cellular processes in development and homeostasis. However, Cdc42's roles in prenatal tooth development remain elusive. Here, we investigated Cdc42 functions in mouse enamel organ. Cdc42 showed highly dynamic temporospatial patterns in the developing enamel organ, with robust expression in the outer enamel epithelium, stellate reticulum (SR), and stratum intermedium layers. Strikingly, epithelium-specific Cdc42 deletion resulted in cystic lesions in the enamel organ. Cystic lesions were first noted at embryonic day 15.5 and progressively enlarged during gestation. At birth, cystic lesions occupied the bulk of the entire enamel organ, with intracystic erythrocyte accumulation. Ameloblast differentiation was retarded upon epithelial Cdc42 deletion. Apoptosis occurred in the Cdc42 mutant enamel organ prior to and synchronously with cystogenesis. Transmission electron microscopy examination showed disrupted actin assemblies, aberrant desmosomes, and significantly fewer cell junctions in the SR cells of Cdc42 mutants than littermate controls. Autophagosomes were present in the SR cells of Cdc42 mutants relative to the virtual absence of autophagosome in the SR cells of littermate controls. Epithelium-specific Cdc42 deletion attenuated Wnt/β-catenin and Shh signaling in dental epithelium and induced aberrant Sox2 expression in the secondary enamel knot. These findings suggest that excessive cell death and disrupted cell-cell connections may be among multiple factors responsible for the observed cystic lesions in Cdc42 mutant enamel organs. Taken together, Cdc42 exerts multidimensional and pivotal roles in enamel organ development and is particularly required for cell survival and tooth morphogenesis.
Topics: Actins; Ameloblasts; Animals; Apoptosis; Autophagosomes; Blotting, Western; Cell Differentiation; Cysts; Cytoskeletal Proteins; Enamel Organ; Epithelium; In Situ Nick-End Labeling; Intercellular Junctions; Mice; Microscopy, Electron, Transmission; Real-Time Polymerase Chain Reaction; rho GTP-Binding Proteins
PubMed: 29874522
DOI: 10.1177/0022034518779546 -
The Japanese Dental Science Review May 2018The continuity of epithelial tissue is collapsed by tooth eruption. The junctional epithelium (JE) is attached to the tooth surface by hemidesmosomes, which constitutes... (Review)
Review
The continuity of epithelial tissue is collapsed by tooth eruption. The junctional epithelium (JE) is attached to the tooth surface by hemidesmosomes, which constitutes the front-line defense against periodontal bacterial infection. JE constitutively expresses intercellular adhesion molecule-1 (ICAM-1), and neutrophils and lymphocytes penetrate into JE via interaction between ICAM-1 and LFA-1 expressed on the surface of these migrating cells. JE also expresses cytokines and chemokines. These functions of JE are maintained even in germ-free condition. Therefore, the constitutive expression of adhesion molecules, cytokines, and chemokines might be used not only for anti-pathogenic defense but also for maintaining the physiological homeostasis of JE. In this review, we have mainly focused on the structural and functional features of JE, and discussed the function of intraepithelial lymphocytes in JE as a front-line anti-microbial defense barrier and regulator of JE hemostasis.
PubMed: 29755616
DOI: 10.1016/j.jdsr.2017.11.004 -
JBMR Plus Mar 2021Micro-computed tomography (μCT) has become essential for analysis of mineralized as well as nonmineralized tissues and is therefore widely applicable in the life... (Review)
Review
Micro-computed tomography (μCT) has become essential for analysis of mineralized as well as nonmineralized tissues and is therefore widely applicable in the life sciences. However, lack of standardized approaches and protocols for scanning, analyzing, and reporting data often makes it difficult to understand exactly how analyses were performed, how to interpret results, and if findings can be broadly compared with other models and studies. This problem is compounded in analysis of the dentoalveolar complex by the presence of four distinct mineralized tissues: enamel, dentin, cementum, and alveolar bone. Furthermore, these hard tissues interface with adjacent soft tissues, the dental pulp and periodontal ligament (PDL), making for a complex organ. Drawing on others' and our own experience analyzing rodent dentoalveolar tissues by μCT, we introduce techniques to successfully analyze dentoalveolar tissues with similar or disparate compositions, densities, and morphological characteristics. Our goal is to provide practical guidelines for μCT analysis of rodent dentoalveolar tissues, including approaches to optimize scan parameters (filters, voltage, voxel size, and integration time), reproducibly orient samples, define regions and volumes of interest, segment and subdivide tissues, interpret findings, and report methods and results. We include illustrative examples of analyses performed on genetically engineered mouse models with phenotypes in enamel, dentin, cementum, and alveolar bone. The recommendations are designed to increase transparency and reproducibility, promote best practices, and provide a basic framework to apply μCT analysis to the dentoalveolar complex that can also be extrapolated to a variety of other tissues of the body. © 2021 The Authors. published by Wiley Periodicals LLC. on behalf of American Society for Bone and Mineral Research.
PubMed: 33778330
DOI: 10.1002/jbm4.10474 -
Frontiers in Physiology 2017Every tissue is composed of multiple cell types that are developmentally, evolutionary and functionally integrated into the unit we call an organ. Teeth, our organs for... (Review)
Review
Every tissue is composed of multiple cell types that are developmentally, evolutionary and functionally integrated into the unit we call an organ. Teeth, our organs for biting and mastication, are complex and made of many different cell types connected or disconnected in terms of their ontogeny. In general, epithelial and mesenchymal compartments represent the major framework of tooth formation. Thus, they give rise to the two most important matrix-producing populations: ameloblasts generating enamel and odontoblasts producing dentin. However, the real picture is far from this quite simplified view. Diverse pulp cells, the immune system, the vascular system, the innervation and cells organizing the dental follicle all interact, and jointly participate in transforming lifeless matrix into a functional organ that can sense and protect itself. Here we outline the heterogeneity of cell types that inhabit the tooth, and also provide a life history of the major populations. The mouse model system has been indispensable not only for the studies of cell lineages and heterogeneity, but also for the investigation of dental stem cells and tooth patterning during development. Finally, we briefly discuss the evolutionary aspects of cell type diversity and dental tissue integration.
PubMed: 28638345
DOI: 10.3389/fphys.2017.00376